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1 ducin repeat-containing protein 2), and APC (adenomatous polyposis coli).
2 ng glycogen synthase kinase 3beta, axin, and adenomatous polyposis coli.
3 genic mechanism associated with mutations in Adenomatous Polyposis Coli.
4 urden in a murine tumor model of spontaneous adenomatous polyposis coli.
7 sly in germ cells for proper localization of Adenomatous polyposis coli 2 and E-cadherin at the hub-G
9 tive regulators of beta-catenin, such as the adenomatous polyposis coli and Axin tumor suppressor pro
10 G-protein signaling (RGS) domain that binds adenomatous polyposis coli and Galpha subunits, thereby
11 that are typically associated with a loss of adenomatous polyposis coli and up-regulation of beta-cat
12 member 1, insulin-like growth factor 2, and adenomatous polyposis coli) and other solid tumors (e.g.
13 of the postsynaptic density, among them the adenomatous polyposis coli, and 2) proteins with express
14 aditionally attributed to mutations in Axin, adenomatous polyposis coli, and beta-catenin that lead t
16 e conditionally expressed a mutant allele of adenomatous polyposis coli (APC(cKO)) in murine uterine
17 n on chronic hypoxia-induced PH, we used the adenomatous polyposis coli (Apc(Min/+)) mouse, where red
18 ve shown that a cancer causing truncation in adenomatous polyposis coli (APC) (APC(1-1450)) dominantl
22 contribution of the Wnt-regulating proteins adenomatous polyposis coli (APC) and APC2 in the pathoge
23 ested that specific GSK3 substrates, such as adenomatous polyposis coli (APC) and collapsin response
24 we show that two tumor suppressor proteins, adenomatous polyposis coli (APC) and Dlg1-SAP97, are req
25 wo microtubule plus end-associated proteins, adenomatous polyposis coli (APC) and EB1, providing a po
26 onal and transcriptional mechanisms and that adenomatous polyposis coli (APC) and GSK3beta, which are
27 expression of the gut tumor suppressor gene adenomatous polyposis coli (Apc) and its role in the oli
28 e, we report that mPar3 forms a complex with adenomatous polyposis coli (APC) and kinesin superfamily
30 associate with the tumor suppressor protein adenomatous polyposis coli (APC) and p150glued, a compon
31 ed by the colorectal cancer tumor suppressor adenomatous polyposis coli (APC) and that KLF4 repressed
32 ther, we find that both the tumor suppressor adenomatous polyposis coli (APC) and the ADP-ribose poly
33 nce microscopy to image the tumor suppressor adenomatous polyposis coli (APC) and the formin mDia1 du
34 firmed an expected loss in the expression of adenomatous polyposis coli (APC) and the transcriptional
35 First, patients with germline mutations in adenomatous polyposis coli (APC) are susceptible to stom
36 polyposis (FAP) but further study identified adenomatous polyposis coli (APC) as responsible for FAP
39 associates with and blocks activation of the adenomatous polyposis coli (APC) destruction complex tha
40 C57BL/6J mice carrying the Min allele of Adenomatous polyposis coli (Apc) develop numerous adenom
42 rectal cancers consistently contained mutant adenomatous polyposis coli (APC) DNA molecules in their
43 show here that the tumor-suppressor protein adenomatous polyposis coli (APC) functions in localizing
45 mice bearing a heterozygote mutation in the adenomatous polyposis coli (APC) gene (Apc(Min/+) mice).
46 ted gene-targeted pigs with mutations in the adenomatous polyposis coli (APC) gene (APC) that are ort
48 of these models involve modification of the adenomatous polyposis coli (Apc) gene and are excellent
49 lasia) mice carry a dominant mutation in the adenomatous polyposis coli (Apc) gene and develop multip
50 hrough somatic second hit alterations of the adenomatous polyposis coli (APC) gene and frequently dem
51 ased in human cells with deficiencies in the adenomatous polyposis coli (APC) gene and in cells stimu
60 l cancer cell lines bearing mutations on the adenomatous polyposis coli (APC) gene as a model of FAP-
62 using a Cre-LoxP strategy to inactivate the Adenomatous Polyposis Coli (Apc) gene in the murine rena
68 ost colorectal cancers have mutations of the adenomatous polyposis coli (APC) gene or the beta-cateni
71 letion in mice with inactivating mutation of adenomatous polyposis coli (APC) gene reduces intestinal
73 in-terminating mutation in one allele of the adenomatous polyposis coli (Apc) gene that is similar to
74 rase beta and in vivo point mutations of the adenomatous polyposis coli (APC) gene that leads to colo
75 ssf1a can cooperate with inactivation of the adenomatous polyposis coli (Apc) gene to accelerate inte
76 ization of beta-catenin or defective for the adenomatous polyposis coli (APC) gene to reinvestigated
78 n the bladder as conditional deletion of the adenomatous polyposis coli (Apc) gene within the adult b
81 intestinal carcinogenesis is mutation of the adenomatous polyposis coli (APC) gene, which leads to ac
82 requently bear inactivating mutations of the adenomatous polyposis coli (APC) gene, whose product is
91 e generated mice lacking the beta-catenin or adenomatous polyposis coli (Apc) genes in osteoblasts.
92 here that the mouse tumor suppressor protein adenomatous polyposis coli (APC) has a role in AChR clus
97 ncluding the brain, and the tumor suppressor adenomatous polyposis coli (APC) is a key negative regul
113 aling following loss of the tumor suppressor adenomatous polyposis coli (APC) is thought to initiate
114 ore, the loss of heterozygosity rates at the adenomatous polyposis coli (Apc) locus are unaffected by
117 vessels in RIP-Tag2 transgenic mouse tumors, adenomatous polyposis coli (apc) mouse adenomas, and imp
119 esis that initiation of colorectal cancer by adenomatous polyposis coli (APC) mutation is mediated by
121 tween up-regulation of VEGF-A expression and adenomatous polyposis coli (APC) mutational status (acti
124 nt/beta-catenin pathway activation caused by adenomatous polyposis coli (APC) mutations occurs in app
127 (CRCs), an initiating mutation occurs in the adenomatous polyposis coli (APC) or beta-catenin gene, a
128 n that have been associated with loss of the adenomatous polyposis coli (APC) or constitutive activat
133 nestin expressing NeuN positive neurons and adenomatous polyposis coli (APC) positive mature oligode
134 in of E-cadherin or a functional fragment of adenomatous polyposis coli (APC) protein (APC-25) comple
137 ibition of GSK-3beta and accumulation of the adenomatous polyposis coli (APC) protein at the plus end
138 ere, we report that the expression status of adenomatous polyposis coli (APC) protein determines the
144 rating cells, and induces the interaction of adenomatous polyposis coli (Apc) protein with the plus e
148 inked to deficiencies in mismatch repair and adenomatous polyposis coli (APC) proteins, diet, inflamm
149 ing a knockout allele in the gatekeeper gene Adenomatous polyposis coli (Apc) recapitulates familial
152 is functionally important for cell migration.Adenomatous polyposis coli (APC) regulates the localizat
153 gene targeting in mice, we demonstrate that adenomatous polyposis coli (APC) serves an essential fun
155 ne such pathway the tumor-suppressor protein adenomatous polyposis coli (APC) targets RNAs to cell pr
156 Here, we have defined a repeat sequence in adenomatous polyposis coli (APC) that binds to EB1's COO
157 ting factor-responsive cells were defined by adenomatous polyposis coli (APC) time-of-flight mass cyt
159 In turn, KIF17 participates in localizing adenomatous polyposis coli (APC) to the plus ends of a s
166 found in patients harboring mutations in the adenomatous polyposis coli (APC) tumor suppressor gene.
172 ce with IEC-specific allelic deletion of the adenomatous polyposis coli (Apc) tumor suppressor locus,
173 atase 2A (PP2A) and must be protected by the adenomatous polyposis coli (APC) tumor suppressor protei
175 rcinomas contain truncating mutations in the adenomatous polyposis coli (APC) tumor suppressor, a neg
176 in signaling is negatively controlled by the adenomatous polyposis coli (APC) tumor suppressor, which
178 calculating the in vivo mutation rate of the adenomatous polyposis coli (APC) tumor-suppressor gene i
179 ollows a genetic pathway whereby loss of the adenomatous polyposis coli (APC) tumour suppressor and a
180 RNAs in the granules associate with the adenomatous polyposis coli (APC) tumour suppressor and t
184 In this study, the tumor suppressor protein adenomatous polyposis coli (APC) was found to be importa
187 ne the genetic relationship between MPC1 and Adenomatous polyposis coli (APC), a key tumor suppressor
189 approaches suggest that the tumor suppressor adenomatous polyposis coli (APC), a regulator of Wnt sig
195 atenin destruction complex components Axin1, adenomatous polyposis coli (APC), and GSK3beta were also
196 gradation complex in vitro, including Dvl-1, adenomatous polyposis coli (APC), axin, and beta-catenin
197 ein complex containing the proteins axin and adenomatous polyposis coli (APC), both of which bind dir
198 forms a complex with axin (axis inhibitor), adenomatous polyposis coli (APC), casein kinase 1alpha (
199 Rac1-specific exchange factor stimulated by adenomatous polyposis coli (APC), contributing to colore
200 Together with its direct binding partner adenomatous polyposis coli (APC), EB1 can stabilize micr
203 in acromegaly patients induced colon p53 and adenomatous polyposis coli (APC), reversing progrowth GH
204 e designed against beta-catenin (Ctnnb1) and adenomatous polyposis coli (Apc), two commonly mutated g
205 ical Wnt signaling by targeting the gene for Adenomatous Polyposis Coli (Apc), which controls Wnt sig
206 e, we show that the tumor suppressor protein adenomatous polyposis coli (APC), which is a known MT-as
207 its expression and activity using models of adenomatous polyposis coli (APC)- and chemotherapy-induc
212 o develop colitis-associated and spontaneous adenomatous polyposis coli (APC)-related tumors of the i
222 ation suppresses beta-catenin activity in an adenomatous polyposis coli (APC)/glycogen synthase kinas
226 I, IGF2; tumor suppressor candidate 33, N33; adenomatous polyposis coli, APC; mut-L homolog 1, MLH1;
227 Arm is targeted for proteolysis by the Axin/Adenomatous polyposis coli (Apc1 and Apc2)/Zeste-white 3
228 a-catenin pathway mutations, such as loss of adenomatous polyposis coli, are insensitive to this nove
229 atenin and the destruction complex component adenomatous polyposis coli at a similar SLS motif to the
230 e glycogen synthase kinase 3beta (GSK3beta)- adenomatous polyposis coli-axin-mediated degradation pat
232 kers associated with colon cancer, including adenomatous polyposis coli, beta-catenin, p53, c-myc, cy
233 coded by the CCND1 gene and activated by the adenomatous polyposis coli-beta-catenin-T-cell factor/ly
234 intestinal tumors driven by mutations in the adenomatous polyposis coli/beta-catenin pathway and acti
237 erived WNT2 activated canonical signaling in adenomatous polyposis coli/beta-catenin wild-type colon
238 V integration site family (WNT)/beta-catenin/adenomatous polyposis coli (CTNNB1/APC) pathway has been
240 otubule organization and capture dynamics in adenomatous polyposis coli-deficient radial progenitors.
241 in cancer cells by restoration of wild type adenomatous polyposis coli function or expression of a d
242 e intestinal neoplasia (Min) mutation of the adenomatous polyposis coli gene (Apc) and homozygous for
243 adic colon adenomas acquire mutations in the adenomatous polyposis coli gene (APC) and show defects i
244 By using mice with germline mutations in the adenomatous polyposis coli gene (Apc) and/or DNA mismatc
246 t human colorectal cancers, mutations in the adenomatous polyposis coli gene (APC) or CTNNB1 constitu
248 iation domain family 1 gene RASSF1A, and the adenomatous polyposis coli gene APC in tumors and in his
249 Mice carrying and non-sense mutation in Adenomatous polyposis coli gene at site R850, which desi
251 olyposis because of germline mutation of the adenomatous polyposis coli gene is characterized by deve
253 its other negative regulators, such as axin, adenomatous polyposis coli gene product (APC), and glyco
254 eta-catenin by inhibiting its binding to the adenomatous polyposis coli gene product and subsequent g
255 in, where carrier proteins like axin and the adenomatous polyposis coli gene product APC interact wit
256 comparatively rare missense variants in the adenomatous polyposis coli gene, which is responsible fo
260 g in T cell lineages by deletion of the Apc (adenomatous polyposis coli) gene causes spontaneous T ce
261 and function through Disheveled (Dvl), Axin, adenomatous polyposis coli, glycogen synthase kinase 3be
262 -catenin pathway regulatory genes, including adenomatous polyposis coli, GSK3beta, axin 1, beta-caten
263 nction of the tumor suppressor protein, APC (adenomatous polyposis coli), in the regulation of base e
264 mutation of the Wnt repressor APC (encoding adenomatous polyposis coli) leads to a state of aberrant
265 that contained mutations in either the APC (adenomatous polyposis coli) locus or in an allele of bet
266 ted signaling and glycogen synthase kinase-3/adenomatous polyposis coli-mediated beta-catenin activat
272 ling induced by loss of the tumor suppressor adenomatous polyposis coli or casein kinase 1alpha uncov
273 Additional examination of one or more of the adenomatous polyposis coli, p14ARF, p16INK4a, or death a
274 Most information about the roles of the adenomatous polyposis coli protein (APC) and its binding
275 at RNAi-mediated depletion of two kMAPs, the adenomatous polyposis coli protein (APC) and its binding
276 olding protein Axin and the tumor suppressor adenomatous polyposis coli protein (APC) are critical co
278 Here we report that the tumour suppressor adenomatous polyposis coli protein (APC) directs the loc
280 d beta-catenin requires interaction with the adenomatous polyposis coli protein but not with TCF for
282 n from Mlp of a region similar to one in the adenomatous polyposis coli protein involved in EB1 bindi
283 ows that the actin-nucleating ability of the adenomatous polyposis coli protein is required for disas
286 versely, RNAi of the beta-catenin antagonist adenomatous polyposis coli results in the regeneration o
288 W480 cells stably transformed with wild-type adenomatous polyposis coli showed decreased beta-catenin
289 on, and beta-catenin, a component of the Wnt-adenomatous polyposis coli signaling pathway, contribute
290 cognized a different autoantigen, except for adenomatous polyposis coli that was recognized by sera o
291 ectly targets the tumor suppressor gene APC (adenomatous polyposis coli), thereby affecting Wnt (Wing
294 he microtubule motor cytoplasmic dynein, the adenomatous polyposis coli tumor suppressor protein (APC
295 centrosome function and cortically localized Adenomatous Polyposis Coli tumor suppressor protein to o
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